Nigrostriatal dopaminergic vulnerability in Parkinson’s disease: Neuroprotective strategies Estefanía Santana-Román, Luis O. Soto-Rojas, Elias Manjarrez, Oscar Arias-Carrión Neural Regeneration Research, 2026 The selective vulnerability of nigrostriatal dopaminergic neurons is a hallmark of Parkinson’s disease and underlies its progressive motor decline. These neurons are uniquely susceptible to degeneration due to their extensive axonal arborization, high energy demands, sustained pacemaking activity, and cytosolic dopamine metabolism, which collectively promote oxidative stress and mitochondrial dysfunction. Advances in single-nucleus RNA sequencing and spatial transcriptomics have revealed transcriptionally distinct dopaminergic subtypes within the human substantia nigra pars compacta, such as AGTR1 + /SOX6 + and RIT2 + populations, which exhibit subtype-specific transcriptional stress signatures and are preferentially lost in Parkinson’s disease. These findings underscore the role of intrinsic vulnerability, influenced by genetic risk loci, mitochondrial stress, and protein misfolding pathways, including α-synuclein aggregation. Furthermore, neuroinflammation, iron accumulation, and vascular dysfunction act synergistically to amplify neuronal loss. This review integrates molecular, cellular, and systems-level mechanisms contributing to dopaminergic degeneration and evaluates emerging neuroprotective strategies. These include anti-oxidative, anti-inflammatory, mitochondrial therapies, novel biomarkers, gene editing, and cell replacement techniques. Understanding the selective vulnerability of nigrostriatal subtypes offers a promising path toward precision-targeted, disease-modifying treatments for Parkinson’s disease.
Restless Legs Syndrome: A Network Model of Iron-Dependent Neuromodulation—A Narrative Review Oscar Arias-Carrión Brain Sciences, 2026 Restless legs syndrome (RLS) is traditionally conceptualized as a dopamine-responsive sensorimotor disorder; however, new evidence suggests a more complex and heterogeneous neurobiological basis. Findings from neuroimaging, genetic studies, circadian biology, and clinical research indicate that dopaminergic dysfunction occurs within a broader context of neuromodulatory imbalance involving iron metabolism, adenosinergic signalling, glutamatergic excitability, and, potentially, noradrenergic pathways. In parallel, quantitative susceptibility mapping and related approaches have provided indirect evidence of altered brain iron distribution, although results remain variable across studies. Clinically, RLS extends beyond nocturnal discomfort and is associated with sleep fragmentation, impaired quality of life, and neuropsychiatric comorbidity, as well as treatment-related complications such as augmentation. However, current diagnostic frameworks remain predominantly phenomenological, and available biomarkers lack sufficient validation for routine clinical use. In this narrative review, the available clinical, genetic, and neuroimaging evidence is synthesized to propose an integrative, network-based model in which iron-dependent neuromodulatory processes influence excitability across cortico–striatal–thalamo–limbic circuits. This framework is intended as a hypothesis-generating model rather than a definitive explanation of disease mechanisms. Substantial heterogeneity across studies, together with variability in clinical presentation and limited reproducibility of candidate biomarkers, underscores the need for standardized methodologies and longitudinal, multimodal investigations. Future work should aim to test this model empirically, refine biological stratification, and determine whether network-informed approaches can improve diagnosis and therapeutic targeting in RLS.
Regulatory Variation at TERT and TERC Shows Limited Association with Early-Onset Alzheimer's Disease in Carriers of the Mexican Founder Mutation PSEN1 A431E Celeste Patricia Gazcón-Rivas, Iliannis Yisel Roa-Bruzón, Luis Félix Duany-Almira, Cesar Aly Valdéz-Gaxiola, Sofia Dumois-Petersen, et al. Medical Sciences Basel Switzerland, 2026 Background: Early-onset Alzheimer’s disease (EOAD) caused by autosomal dominant mutations provides a deterministic framework for investigating genetic modifiers of neurodegeneration. Telomere biology has emerged as a central regulator of genomic stability, cellular ageing, and stress response integration, yet its role in EOAD, particularly in under-represented populations, remains poorly defined. Methods: We conducted a cross-sectional case–control study to evaluate the genetic distribution, disease association, and predicted regulatory consequences of common variants in the telomere maintenance genes TERT and TERC in individuals from Western Mexico. The EOAD group comprised genetically confirmed carriers of the PSEN1 p.Ala431Glu (A431E) founder mutation with clinical EOAD (n = 69), and controls were unrelated individuals without dementia (n = 179). Five common variants were analyzed: rs2242652, rs2853677, rs2736100, and rs10069690 (TERT), and rs12696304 (TERC). Results: Genotype distributions in controls conformed to the Hardy–Weinberg equilibrium. Single-variant analyses showed no significant allele-level associations. Most TERT variants did not show significant allele-level associations with EOAD. However, a preliminary genotype-level enrichment for the GC allele at rs12696304 (TERC) was observed among EOAD cases compared with controls; allele-level associations were not significant. Linkage disequilibrium analysis revealed low r2 values (<0.20), supporting variant independence. Population-level allele frequency comparisons revealed ancestry-dependent divergence across loci; in silico functional annotation localised all variants to non-coding regulatory regions. GTEx-based analyses indicated that rs12696304 acts as an eQTL for ACTRT3 in whole blood and pituitary, as well as for LRRC34 in the cerebellar hemisphere, suggesting a potential regulatory network within the TERC locus (3q26.2). Conclusions: Overall, common regulatory variants in TERT did not show strong independent effects on EOAD susceptibility in PSEN1 A431E carriers. However, the convergence of association patterns, functional annotation, and regulatory evidence provides hypothesis-generating support for the TERC locus (3q26.2), particularly rs12696304, as a candidate region for further investigation. Additional studies integrating telomere dynamics, functional validation, and multi-omics analyses are needed to clarify the role of telomere biology in the pathogenesis of autosomal dominant EOAD.
Quantum-Inspired and Non-Classical Approaches to Consciousness: Models, Evidence and Constraints Oscar Arias-Carrión, Emmanuel Ortega-Robles, Elías Manjarrez Brain Sciences, 2026 Consciousness presents a structural puzzle: a unified, context-sensitive, globally integrated mode of experience emerging from distributed neural dynamics. While classical neuroscience has mapped synaptic, oscillatory, and network-level mechanisms with increasing precision, debate persists as to whether classical formalisms fully capture the integrative and contextual features of conscious processing. This review examines whether quantum principles offer explanatory leverage in two distinct senses: as formal mathematical frameworks for modeling contextual cognition, and as mechanistic hypotheses proposing biologically instantiated non-classical states. We surveyed empirical and theoretical developments spanning zero-quantum-coherence in MRI signals, entanglement-structured learning paradigms, quantum-inspired computational models, and proposed neural substrates, including microtubules, nuclear spins, and photonic architectures. Although certain findings have been interpreted as consistent with a non-classical structure, no study to date has demonstrated entanglement, long-lived coherence, or collapse dynamics in neural tissue under operational criteria comparable to those used in controlled quantum systems. Replication remains limited, biological entanglement witnesses are not yet established, and nonlinear classical dynamics can reproduce many putative quantum signatures. Accordingly, the decisive question is not whether the brain is quantum, but whether its dynamics exceed the explanatory reach of rigorously defined classical models. Progress hinges on replication, adversarial scrutiny, and operational criteria precise enough to discriminate genuine non-classical correlations from classical complexity. Whether quantum mechanisms ultimately prove necessary or refined classical models remain sufficient, this inquiry compels a deeper understanding of integration, contextuality, and the physical constraints shaping conscious experience.
Parkinson’s Disease: From Gene–Environment Risk to Precision Therapy Oscar Arias-Carrión Medical Sciences, 2026 Parkinson’s disease (PD) is a progressive and heterogeneous neurodegenerative disorder and one of the fastest-growing causes of neurological disability worldwide. Although historically defined by motor manifestations resulting from nigrostriatal dopaminergic degeneration, PD is now recognized as a multisystem disorder. Non-motor features—including autonomic dysfunction, neuropsychiatric symptoms, cognitive impairment, and sleep-related disorders—frequently precede motor onset by years or even decades, delineating a clinically meaningful prodromal phase. The aetiology of PD reflects a complex interplay between genetic susceptibility and environmental exposures. Approximately 20% of cases are linked to identifiable pathogenic variants, most commonly in LRRK2, GBA1, and SNCA, whereas the majority arise from cumulative interactions among environmental factors, lifestyle determinants, and common genetic risk variants rather than from single causal mechanisms. Despite substantial advances in understanding disease biology, current therapies remain fundamentally symptomatic. Dopaminergic pharmacotherapy and device-aided interventions improve motor function and, in selected contexts, functional outcomes, but they do not modify disease progression. Non-motor symptoms remain a dominant driver of disability and reduced quality of life. Recent conceptual frameworks propose redefining PD as a biologically defined α-synucleinopathy. Emerging biomarkers, including α-synuclein seed amplification assays in cerebrospinal fluid and peripheral tissues, offer unprecedented opportunities to define biological disease, enable early detection, and stratify patients. However, biomarker positivity currently informs diagnosis and classification rather than prognostication or therapeutic selection, and validated intermediate endpoints linking biomarker change to sustained functional benefit remain lacking. Consequently, translation into disease-modifying therapies has been constrained by late-stage intervention, reliance on clinically defined populations, limited trial generalizability, and marked global inequities in access to advanced diagnostics and treatments. This narrative review synthesizes current evidence on PD epidemiology, diagnosis, aetiology, progression, and treatment, emphasizing gene–environment interactions, convergence on shared pathogenic pathways, limitations of existing therapeutic paradigms, and the as-yet unrealized potential of biologically informed precision care.
Optimizing Hoffmann Reflex Rate-Dependent Depression: A Feasible Protocol for Assessing Spinal Inhibition in Upper and Lower Limbs Andrea S. Ceñal Cisneros, Rodolfo Delgado-Lezama, Carlos A. Cuellar, Oscar Arias-Carrión, Isabel Ruelas Galindo, et al. Medical Sciences, 2026 Background: Rate-dependent depression of the Hoffmann reflex (RDD-HR) is a neurophysiological marker of spinal inhibition altered in several neurological conditions, yet no consensus exists on optimal stimulation frequency, number of stimuli, or the feasibility of upper limb recordings. This study aimed to define practical, standardized parameters for reliable RDD-HR assessment in upper and lower limbs of healthy adults, as a first step toward clinical application. Methods: In this observational study, bilateral Hoffmann reflexes were recorded from the flexor carpi radialis and soleus muscles in 21 healthy adults. Stimulation was delivered using three 10-pulse trains at seven frequencies (0.1–5 Hz). RDD-HR was quantified as the median H-reflex area, expressed as a percentage of the first response (lower values indicate greater depression). Optimal frequencies and minimal stimuli were identified by sigmoid fitting and confidence analyses, with train and stimulus effects tested by two-way ANOVA. Results: RDD-HR displayed a sigmoidal frequency–response across all limbs. Maximal depression occurred at 1–5 Hz, with no significant differences between these frequencies, supporting 1 Hz as optimal. Depression was greater in lower limbs (~30%) than upper limbs (~47%). Reliable estimates were obtained using a single train of seven stimuli, with no benefit from averaging across trains. Upper limb recordings required lower stimulation intensities. Conclusions: RDD-HR can be reliably assessed using a simplified protocol based on a single seven-pulse train at two key frequencies. This standardized approach provides a methodological foundation for future clinical validation of RDD-HR as a biomarker of spinal inhibitory dysfunction.
L-Alliin Modulates Brain Region-Specific Neuroinflammatory Responses to Lipopolysaccharide in Diet-Induced Obese Mice Celia González-Castillo, Daniel Ortuño-Sahagún, Carolina Guzmán-Brambila, Daniel Ulises Torres-Reyes, Lucrecia Carrera-Quintanar, et al. Brain Sciences, 2026 Background/Objectives: A high-fat diet disrupts metabolic and neuroimmune balance in the brain, making neural tissue more reactive to inflammatory challenges. However, it is not well understood how this vulnerability varies across brain regions or how natural anti-inflammatory compounds influence it. Methods: In this study, we examined how the garlic-derived molecule L-alliin modulates the inflammatory response triggered by lipopolysaccharide in the frontal cortex, hippocampus, and hypothalamus of mice fed either a standard or high-fat diet. Results: Measurements of cytokine gene expression showed that the high-fat diet greatly increased the inflammatory response in the frontal cortex and hypothalamus, with the hypothalamus displaying the strongest overall activation. Treatment with L-alliin significantly reduced elevated cytokine levels in both regions, with the reductions most pronounced in animals on the high-fat diet. In contrast, the hippocampus showed a distinct pattern: expression of TNF-α and IL-1β changed very little across diets or treatments, whereas IL-6 and CCL2 were selectively altered by L-alliin, depending on the animals’ metabolic state. Conclusions: These findings demonstrate that diet-induced obesity does not affect the entire brain uniformly. Instead, inflammatory pathways are altered region-specifically, and L-alliin modulates these pathways with sensitivity to both brain region and metabolic condition. This work emphasizes the importance of accounting for neuroanatomical differences when developing strategies to reduce inflammation in obesity-associated conditions.
Orexin Restoration in Narcolepsy: Breakthroughs in Cellular Therapy Emmanuel Ortega‐Robles, Magdalena Guerra‐Crespo, Shahd Ezzeldin, Estefanía Santana‐Román, Artur Pałasz, et al. Journal of Sleep Research, 2026 Narcolepsy is a chronic neurodegenerative disorder defined by the selective loss of orexin‐producing neurons in the lateral hypothalamus, leading to excessive daytime sleepiness and cataplexy. While pharmacological therapies have evolved to mitigate symptoms, they fail to address the core pathology—orexin deficiency. This narrative review examines the potential of orexin cell transplantation as an innovative therapeutic approach to restore orexin signalling and treat the root cause of narcolepsy. We begin by examining the clinical features, pathophysiology, and diagnostic criteria of narcolepsy, focusing on the essential role of orexins in regulating the sleep–wake cycle and the neurobiological mechanisms underlying cataplexy. The review then explores experimental therapeutic approaches, including hypothalamic tissue grafts, gene therapy, and immortalised orexin‐expressing cell lines, highlighting their potential to address the orexin deficit in narcolepsy. While preclinical studies show that transplanted orexin cells can integrate into host neural networks, enhance sleep stability, and decrease the frequency of cataplexy in animal models, several challenges remain. Immortalised orexin cell lines offer a scalable and consistent option for transplantation therapies. However, immune rejection, long‐term cell survival, and complete functional integration persist. These translational hurdles must be addressed to bring these therapies to clinical practice. This review underscores the need for continued research to overcome these barriers and optimise cell‐based therapies for narcolepsy.
Innate immune signalling, neuroinflammation and network plasticity in temporal lobe epilepsy Oscar Arias-Carrión, Julieta Rodríguez de Ita, Philipp Yu Frontiers in Pharmacology, 2026 Temporal lobe epilepsy emerges from a cascade of molecular, cellular, and structural disturbances triggered by heterogeneous cerebral insults—including convulsive status epilepticus, viral encephalitis, traumatic brain injury, and blood–brain barrier disruption—that converge on progressive hippocampal reorganization and a chronic predisposition to unprovoked focal seizures. Convergent evidence from chemoconvulsant models, focal intrahippocampal kainate administration, viral encephalitis paradigms, organotypic hippocampal cultures, human iPSC-derived organoids, and resected human tissue shows that innate immune pathways are not secondary epiphenomena but central drivers of epileptogenesis. Pattern-recognition receptors—particularly TLR2, TLR3, TLR4, IL-1R1 and the NLRP3 inflammasome—sense pathogen- and damage-associated molecular motifs, including HMGB1, and initiate MyD88-, NF-κB- and caspase-1–dependent signaling. These cascades acutely amplify IL-1β, TNF-α and IL-6 responses, alter ion-channel phosphorylation states, enhance NMDA- and AMPA-receptor–mediated excitation, and impair GABAergic inhibition, thereby lowering the seizure threshold. Sustained innate immune activation drives microglial M1 polarization, complement-mediated synaptic loss, aberrant neurogenesis, endothelial dysfunction, and persistent astroglial reactivity—mechanisms that reinforce circuit hyperexcitability and enable the transition from provoked to spontaneous recurrent seizures. Targeted interventions—including TLR4 antagonists (TAK-242), IL-1–pathway inhibitors (anakinra; the caspase-1 inhibitor VX-765), NLRP3 inhibitors (MCC950), and complement-directed strategies—reduce seizure burden, mitigate hippocampal atrophy, and, when administered early, attenuate maladaptive network remodeling. Several conventional antiseizure medications, including levetiracetam, also exhibit immunomodulatory properties by modulating microglial activation, suggesting a mechanistic overlap between pharmacological seizure control and immune regulation. Emerging data implicate the TLR7–endogenous retrovirus axis as an upstream determinant of neuroimmune homeostasis, linking impaired surveillance of viral and retroelement activity to glial activation and network instability. Together, these findings position innate immunity as a mechanistically coherent and therapeutically tractable axis in temporal lobe epilepsy. Achieving clinical translation will require immune-phenotype stratification, biomarker-guided timing of intervention, and advances in CNS-targeted delivery. Integrating immunomodulatory approaches with established antiseizure therapies offers a promising route toward disease modification, cognitive preservation, and more precise treatment of drug-resistant epilepsy.
Redefining Non-Motor Symptoms in Parkinson’s Disease Laura Peña-Zelayeta, Karen M. Delgado-Minjares, Marcos M. Villegas-Rojas, Karen León-Arcia, Alberto Santiago-Balmaseda, et al. Journal of Personalized Medicine, 2025
Alzheimer’s Disease: Understanding Motor Impairments Jesús Andrade-Guerrero, Humberto Martínez-Orozco, Marcos M. Villegas-Rojas, Alberto Santiago-Balmaseda, Karen M. Delgado-Minjares, et al. Brain Sciences, 2024
Dopaminergic modulation of sleep-wake states Andrea Herrera-Solis, Wendy Herrera-Morales, Luis Nunez-Jaramillo, Oscar Arias-Carrion CNS and Neurological Disorders Drug Targets, 2017
Nanomaterials for neurology: State-of-the-art María Veloz-Castillo, Rachel West, Jessica Cordero-Arreola, Oscar Arias-Carrión, Miguel Méndez-Rojas CNS and Neurological Disorders Drug Targets, 2016
Prior acute mental exertion in exercise and sport Fernando Lopes e Silva-Júnior, Patrick Emanuel, Jordan Sousa, Matheus Silva, Silmar Teixeira, et al. Clinical Practice and Epidemiology in Mental Health, 2016
Treatment of cognitive deficits in Alzheimer's disease: A psychopharmacological review Psychiatria Danubina, 2016
Neurological aspects of grief Adriana Silva, Natalia Ribeiro, Alexandre Schier, Oscar Arias-Carrion, Flavia Paes, et al. CNS and Neurological Disorders Drug Targets, 2014
Caffeine and suicide: A systematic review Adriana Silva, Natalia Ribeiro, Alexandre Schier, Valeska Pereira, Marina Vilarim, et al. CNS and Neurological Disorders Drug Targets, 2014
Sex therapy for female sexual dysfunction Valeska Pereira, Oscar Arias-Carrión, Sergio Machado, Antonio Nardi, Adriana Silva International Archives of Medicine, 2013
Commentary Ying Cui, Jiang Li, Oscar Arias-Carrin, Ti-Fei Yuan CNS and Neurological Disorders Drug Targets, 2012
Clinical implication of Meissner's corpuscles Jose A. Vega, Alfonso Lopez-Muniz, Marta G. Calavia, Olivia Garcia-Suarez, Juan Cobo, et al. CNS and Neurological Disorders Drug Targets, 2012
Basic sleep mechanisms: An integrative review Eric Murillo-Rodriguez, Oscar Arias-Carrion, Abraham Zavala-Garcia, Andrea Sarro-Ramirez, Salvador Huitron-Resendiz Central Nervous System Agents in Medicinal Chemistry, 2012
Mechanisms of sleep-wake cycle modulation Eric Murillo-Rodriguez, Oscar Arias-Carrion, Katya Sanguino-Rodriguez, Mauricio Gonzalez-Arias, Reyes Haro CNS and Neurological Disorders Drug Targets, 2009
帕金森病黑质纹状体多巴胺能的易感性: 神经保护策略 E Santana-Román, LO Soto-Rojas, E Manjarrez, O Arias-Carrión 中国神经再生研究 (英文版) 21 (8), 3378 , 2026 2026
Nigrostriatal dopaminergic vulnerability in Parkinson’s disease: Neuroprotective strategies E Santana-Román, LO Soto-Rojas, E Manjarrez, O Arias-Carrión Neural Regeneration Research 21 (8), 3378-3386 , 2026 2026 Citations: 6
Walking as a Window to the Brain: Redefining Gait in Neurology E Ortega-Robles, M Treviño, E Manjarrez, O Arias-Carrión Preprints , 2026 2026
Treatment strategies for motor O Arias-Carrión, E Ortega-Robles Advances in Novel Pharmacotherapeutics and Drug Discovery: Computational … , 2026 2026
Regulatory Variation at TERT and TERC Shows Limited Association with Early-Onset Alzheimer’s Disease in Carriers of the Mexican Founder Mutation PSEN1 A431E CP Gazcón-Rivas, IY Roa-Bruzón, LF Duany-Almira, CA Valdéz-Gaxiola, ... Medical Sciences 14 (2), 228 , 2026 2026
Safety and preliminary efficacy of Aurora: a pilot, non-randomized clinical trial of a culturally adapted digital cognitive behavioral therapy intervention for anxiety and … E Zárate, AC Velasco-Téllez, LA Sanchez-Reyes, ÁM Coll-Muñoz, ... Frontiers in Psychiatry 17, 1824079 , 2026 2026
The Hoffmann Reflex O Arias-Carrión, E Ortega-Robles Preprints , 2026 2026
Restless Legs Syndrome: A Network Model of Iron-Dependent Neuromodulation—A Narrative Review O Arias-Carrión Brain Sciences 16 (5), 440 , 2026 2026
Narcolepsy as an immune-associated hypothalamic encephalopathy: orexin dysfunction and implications for precision sleep medicine O Arias-Carrión, E Ortega-Robles, P Romano, C Pineda Frontiers in Psychiatry 17, 1799520 , 2026 2026
Age-related synaptic vesicle dysfunction as a prodromal target in Parkinson’s disease: Mechanistic insights from alpha-synuclein biology O Arias-Carrión Aging Advances 3 (2), 82-89 , 2026 2026
Quantum-Inspired and Non-Classical Approaches to Consciousness: Models, Evidence and Constraints O Arias-Carrión, E Ortega-Robles, E Manjarrez Brain Sciences 16 (4), 386 , 2026 2026 Citations: 4
Structural shifts and constraints in animal-based neuroscience M Treviño, O Arias-Carrión Academia Neuroscience and Brain Research 2 (1) , 2026 2026
L-Alliin Modulates Brain Region-Specific Neuroinflammatory Responses to Lipopolysaccharide in Diet-Induced Obese Mice C González-Castillo, D Ortuño-Sahagún, C Guzmán-Brambila, ... Brain Sciences 16 (2), 243 , 2026 2026
The genetic architecture of Parkinson's disease in Mexico: a systematic review O Arias-Carrión, E Romero-Gutiérrez, FX Castellanos-Juárez, ... Frontiers in Aging Neuroscience 18, 1709246 , 2026 2026
Innate immune signalling, neuroinflammation and network plasticity in temporal lobe epilepsy O Arias-Carrion, JR de Ita, P Yu Frontiers in Pharmacology 17, 1770964 , 2026 2026
Parkinson’s Disease: From Gene–Environment Risk to Precision Therapy O Arias-Carrión Medical Sciences 14 (1), 72 , 2026 2026 Citations: 2
Public Health Education in Mexico in 2024: National Distribution, Accreditation, and Modalities of Training J Real-Ramírez, O Arias-Carrión Journal of Mind and Medical Sciences 13 (1), 4 , 2026 2026
Noise-Limited Failure of OGY Chaos Control in Regulating Monosynaptic Reflex Variability in the In Vivo Cat Spinal Cord E Manjarrez, I Méndez-Balbuena, SM Dominguez-Nicolas, ... NeuroSci 7 (1), 18 , 2026 2026
Orexin restoration in narcolepsy: breakthroughs in cellular therapy E Ortega‐Robles, M Guerra‐Crespo, S Ezzeldin, E Santana‐Román, ... Journal of Sleep Research 35 (1), e70083 , 2026 2026 Citations: 3
Physical exercise mitigates motor and muscular deficits in the 3xTg-AD model of Alzheimer’s disease J Andrade-Guerrero, K León-Arcia, OE Aparicio-Trejo, B Cuevas-López, ... Frontiers in Aging Neuroscience 18, 1730578 , 2026 2026
MOST CITED SCHOLAR PUBLICATIONS
Dopaminergic reward system: a short integrative review O Arias-Carrión, M Stamelou, E Murillo-Rodríguez, ... International archives of medicine 3 (1), 1-6 , 2010 2010 Citations: 784
Effects of Exercise on Anxiety and Depression Disorders: Review of Meta- Analyses and Neurobiological Mechanisms M Wegner, I Helmich, S Machado, A E Nardi, O Arias-Carrion, H Budde CNS & Neurological Disorders-Drug Targets 13 (6), 1002-1014 , 2014 2014 Citations: 725
Dopamine, learning, and reward-seeking behavior. Ó Arias-Carrión, E Pöppel Acta Neurobiol Exp , 2007 2007 Citations: 525
Epidemiology of early-onset dementia RT Vieira, L Caixeta, S Machado, AC Silva, AE Nardi, O Arias-Carrión, ... Clinical practice and epidemiology in mental health: CP & EMH 9, 88 , 2013 2013 Citations: 494
Handbook of cannabis RG Pertwee Oxford University Press, USA , 2014 2014 Citations: 421
Sleep deprivation and oxidative stress in animal models: a systematic review G Villafuerte, A Miguel-Puga, E Murillo Rodríguez, S Machado, ... Oxidative medicine and cellular longevity 2015 (1), 234952 , 2015 2015 Citations: 369
Antidepressant-Like and Anxiolytic-Like Effects of Cannabidiol: A Chemical Compound of Cannabis sativa A R de Mello Schier, N P de Oliveira Ribeiro, D S Coutinho, S Machado, ... CNS & Neurological Disorders-Drug Targets 13 (6), 953-960 , 2014 2014 Citations: 238
The role of positive emotion and contributions of positive psychology in depression treatment: systematic review V Santos, F Paes, V Pereira, O Arias-Carrión, AC Silva, MG Carta, ... Clinical practice and epidemiology in mental health: CP & EMH 9, 221 , 2013 2013 Citations: 222
EEG-based brain-computer interfaces: an overview of basic concepts and clinical applications in neurorehabilitation S Machado, F Araújo, F Paes, B Velasques, M Cunha, H Budde, LF Basile, ... Reviews in the Neurosciences 21 (6), 451-468 , 2010 2010 Citations: 178
A new dopaminergic nigro-olfactory projection GU Höglinger, D Alvarez-Fischer, O Arias-Carrión, M Djufri, A Windolph, ... Acta Neuropathologica 130 (3), 333-348 , 2015 2015 Citations: 161
The mirror neuron system in post-stroke rehabilitation D Carvalho, S Teixeira, M Lucas, TF Yuan, F Chaves, C Peressutti, ... International archives of medicine 6 (1), 1 , 2013 2013 Citations: 156
Neurogenesis in the subventricular zone following transcranial magnetic stimulation and nigrostriatal lesions O Arias‐Carrión, L Verdugo‐Díaz, A Feria‐Velasco, D Millán‐Aldaco, ... J Neurosci Res 78 (1), 16-28 , 2004 2004 Citations: 152
Rational therapeutic approaches to progressive supranuclear palsy M Stamelou, R de Silva, O Arias-Carrión, E Boura, M Höllerhage, ... Brain 133 (6), 1578-1590 , 2010 2010 Citations: 138
Implications of DNA methylation in Parkinson’s disease E Miranda-Morales, K Meier, A Sandoval-Carrillo, J Salas-Pacheco, ... Frontiers in molecular neuroscience 10, 225 , 2017 2017 Citations: 134
Physical activity interventions in schools for improving lifestyle in European countries G Mura, NBF Rocha, I Helmich, H Budde, S Machado, M Wegner, ... Clinical practice and epidemiology in mental health: CP & EMH 11 (Suppl 1 M5 … , 2015 2015 Citations: 121
Carboxymethyl cellulose coated magnetic nanoparticles transport across a human lung microvascular endothelial cell model of the blood–brain barrier G Aguilera, CC Berry, RM West, E Gonzalez-Monterrubio, ... Nanoscale Advances 1 (2), 671-685 , 2019 2019 Citations: 114
Systemic administration of neuregulin‐1β1 protects dopaminergic neurons in a mouse model of Parkinson’s disease T Carlsson, FR Schindler, M Höllerhage, C Depboylu, O Arias‐Carrión, ... Journal of Neurochemistry 117 (6), 1066-1074 , 2011 2011 Citations: 114
Possible involvement of complement factor C1q in the clearance of extracellular neuromelanin from the substantia nigra in Parkinson disease C Depboylu, MKH Schäfer, O Arias-Carrión, WH Oertel, E Weihe, ... Journal of Neuropathology & Experimental Neurology 70 (2), 125-132 , 2011 2011 Citations: 112
Basic sleep mechanisms: an integrative review E Murillo-Rodríguez, O Arias-Carrión, A Zavala-García, A Sarro-Ramírez, ... Central Nervous System Agents in Medicinal Chemistry (Formerly Current … , 2012 2012 Citations: 106
Oxidative stress and adult neurogenesis TF Yuan, S Gu, C Shan, S Marchado, O Arias-Carrión Stem Cell Reviews and Reports 11 (5), 706-709 , 2015 2015 Citations: 104
